CHICAGO—Researchers reported notable advances in the war on cancer over the weekend, including treatments for lung, ovarian and skin cancers, but they cautioned that the disease continues to throw up daunting obstacles of cost and complexity.

New data presented at a major cancer conference provided both practice-changing information on the use of current treatments and powerful evidence of the potential for so-called targeted therapies, which attack cancer via genetic targets and other vulnerabilities.

They also underscore the growing realization that cancer is not a single disease or even a single disease within each location in the body—say, breast, brain or lung. The more scientists know about genes, proteins and pathways that drive cancer, the more complex a disease it becomes.

"Cancer is like cable television," says George Sledge, a breast-cancer expert at Indiana University and newly elected president of the American Society of Clinical Oncology, which hosted the cancer meeting. "Thirty years ago you had three channels. Now you have 500."

The challenge for cancer researchers increasingly is to match the right drug with the right channel.

Sometimes that means going after a tumor directly, aided by genetic anomalies that make a tumor resistant to treatment in one patient but sensitive to it in another.

In one tantalizing example at the meeting, researchers said a drug being developed by Pfizer Inc., called crizotinib, caused tumors to shrink or stabilize in 90% of 82 lung-cancer patients specially recruited for the study because they had an alteration in a gene known as ALK.

Tumors shrank more than 30% in 57% of the patients. While there wasn't a control arm in the study, researchers said the participants had undergone several previous treatments. Normally just 10% of such patients not screened for this genetic anomaly would have been expected to register a response to the treatment.

Lung cancer is the most common cause of cancer death among men and women, but only a 4% of the 220,000 Americans diagnosed with the disease each year have the genetic anomaly—or roughly 10,000 patients.

That significantly reduces the size of the potential lung-cancer market for the study, but it is larger than many other cancers.

Pfizer has already begun a larger study of the drug focusing on those patients to determine whether the drug will help prolong survival.

In another study, Roche Holding AG's drug Avastin, which works by starving tumors of their blood supply, extended the time women with ovarian cancer survived without progression of their disease by four months, to 14 months, when continued for up to two years after a regimen that included Avastin and chemotherapy together.

Ovarian is a particularly deadly cancer for women. Roche said the results were among the first to show a benefit for long-term use of Avastin.

But Avastin in the U.S. costs up to $56,000 a year, and such findings are certain to raise the question whether the benefit is worth the price.

"We have to think about the cost of therapy in the same way we think about long-term side effects," said Jennifer Obel, an oncologist at North Shore University Health System in Illinois.

The latest findings underscore the growing realization that cancer is not a single disease or even a single disease within each location in the body—say, breast, brain or lung.

The more scientists know about genes, proteins and pathways that drive cancer, the more complex a disease it becomes.

Another advance came in a study of a drug called ipilimumab, being developed by Bristol-Myers Squibb Co., that works not by attacking the tumor but by activating the body's immune system to go after the cancer.

In a study of 676 patients with an advanced stage of the deadly skin cancer melanoma, patients taking the medicine lived an average of 10 months compared with 6.5 months for those taking a cancer vaccine called gp100.

The findings reflect growing interest in a variety of approaches to marshal the body's immune system in the fight against cancer.

Bristol-Myers expects to file for marketing approval with the Food and Drug Administration later this year and is studying the medicine in other cancers.

But such advances have been offset by setbacks described in research at the meeting and in other recent findings that illustrate cancer's complexity.

A study of Eli Lilly & Co'.s Erbitux is one example. Two years ago, researchers found that Erbitux improved survival in patients with colon cancer that had spread or metastasized, as long as they had a normal copy of a gene called KRAS.

The expectation was that the drug would also have a benefit earlier in the disease process, for patients with the same normal KRAS gene whose cancer hadn't yet spread.

But a 1,760-patient study found no survival advantage for patients given Erbitux plus chemotherapy, compared with those given chemotherapy alone. "Maybe early-stage colon cancer is a different disease than late-stage disease," Dr. Obel observed.

In another case, Pfizer's Sutent, a significant advance in the treatment of kidney cancer when it came out in 2006, failed in studies presented at the meeting to improve a measure of survival in breast-cancer patients. The company continues to study the medicine in other tumors, including those in the lung and prostate.

The hope was that each of these targeted treatments, which block markers present in a variety of tumor types, would prove successful against more types of cancers.

Roche executives were pleased with newly demonstrated benefits of Avastin in ovarian cancer.

The advances "bring hope, but they also remind us that we need to remain humble in this fight against cancer," said Pascal Soriot, chief operating officer of Roche Group's pharmaceutical business. "It's going to take time and a lot of money before we get a cure."

A decade ago, a drug called Gleevec from Novartis SA electrified the cancer world with its ability to all but cure a deadly form of leukemia thanks to its effect on an aberrant gene known as the Philadelphia chromosome.

It helped transform cancer research into a hunt for genes and other biomarkers that might direct drug development and guide doctors in selecting treatments for their patients.

At the meeting, study data showed that two second-generation drugs—Sprycel from Bristol-Myers Squibb and Tasigna, also from Novartis—outperformed Gleevec in certain measures of treating chromic myelogenous leukemia.

Assuming the drugs, now approved for patients who fail on Gleevec, gain approval for first-line treatment, physicians and patients will have alternatives to one of cancer's iconic drugs.

Gleevec "was such a revolutionary step," says Robert Mayer, vice president for academic affairs at Dana-Farber Cancer Institute, Boston. "It is encouraging that we can find ways to improve the product."

Meantime, the hunt for other strategies for matching drugs to targets continues in earnest.

Among them: Researchers are beginning to use the ability to unravel the genetic sequence of tumors to determine which pathways are active no matter where they're located in the body.

Then they plan to match the patients with already approved drugs, no matter what type of cancer they're on the market for.

CHICAGO — Updated results from the BRAIN study showed that there were no new safety signals and 16% of patients with relapsed glioblastoma treated with bevacizumab plus irinotecan were alive at 2.5 years.

Timothy Cloughesy, MD, director of the UCLA Neuro-Oncology Program at the Ronald Reagan UCLA Medical Center, updated results first presented in 2007 during the 2010 ASCO Annual Meeting.

BRAIN is a phase 2, open-label, multicenter, randomized, non-comparative trial evaluating bevacizumab (Avastin, Genentech) alone or in combination with irinotecan for glioblastoma at first or second relapse. Eighty-five patients were assigned bevacizumab monotherapy and 82 were assigned combination treatment. Eligible patients in the bevacizumab arm who progressed were allowed to crossover to the combination arm in the post-progression phase.

Cloughesy said safety data was little changed from the previous presentation. Grade-3/grade-4 hypertension was 10.7% in the monotherapy group vs. 3.8% in the combination group and 0% in the crossover arm.

At 30 months, 11% of patients in the monotherapy group were still alive compared with 16% in the combination group. Median OS was 9.3 months in the bevacizumab arm vs. 8.9 months in the combination arm. – by Jason Harris

After decades of struggle against all forms of cancer, we finally recorded the first very significant results. The National Cancer Institute published the results of its latest study: mortality is declining. According to the figures, a person with cancer two will be alive after 5 years and nearly 40% of those currently affected by a cancer cure.

These figures are very different in the various forms of cancer. These forms are classified into three different groups; good prognosis, intermediate prognosis and poor prognosis.

For cancers classified as “good prognosis” is more than 40% of cancers, the probability of survival at 5 years exceeds 80%. In this category are melanoma, lymphocytic leukemia or cancer of the breast.

Cancers classified as “intermediate prognosis” have a survival rate at 5 years ranges from 20 to 80%. Included in this category colorectal cancer, ovarian cancer, cancer of the bladder etc.. They represent about 33% of cancers reported and the life expectancy varies greatly depending on the time of screening and the type of cancer.

Cancers have poor prognoses them a hope of survival at 5 years less than 20% Not surprisingly, one finds the lung, pancreas, brain tumors or pleural. For the record, it should be remembered that lung cancers are the leading cause of cancer mortality in Europe, men and women.

These figures, taken in totality, show a marked improvement over the last twenty years. They remain very contrasting forms of lung cancer saw their survival rate will increase only very minimal. However, real progress was made on the forms of cancers where mass screening campaigns have been organized. Medical authorities the often-repeated: cancer can be treated much better it is detected and treated early.

Therapeutic advances are still to be taken into account and some tracks are very promising: decoding DNA tumor progresses to consider more effective treatments for personalized and tailored to only those cell types. Other treatments are designed not to eradicate the cancer but to prevent it from developing, transforming even the chronic but under control. Finally, DNA RNA research provides the first experimental results very satisfactory and opens the way for new therapies very successful on certain forms of cancer.

The war against cancer is not yet won but the medical records now real victories.

Turning a Painkiller Into a Cancer Killer: Pain Reliever Redirected to Trigger Death Pathways in Cancer Cells

ScienceDaily (June 14, 2010) — Without knowing exactly why, scientists have long observed that people who regularly take non-steroidal anti-inflammatory drugs (NSAIDs) like aspirin have lower incidences of certain types of cancer. Now, in a study appearing in Cancer Cell on June 15, investigators at Sanford-Burnham Medical Research Institute (Sanford-Burnham) and their colleagues have figured out how one NSAID, called Sulindac, inhibits tumor growth.

The study reveals that Sulindac shuts down cancer cell growth and initiates cell death by binding to nuclear receptor RXRα, a protein that receives a signal and carries it into the nucleus to turn genes on or off.

"Nuclear receptors are excellent targets for drug development," explained Xiao-kun Zhang, Ph.D., professor at Sanford-Burnham and senior author of the study. "Thirteen percent of existing drugs target nuclear receptors, even though the mechanism of action is not always clear."

RXRα normally suppresses tumors, but many types of cancer cells produce a truncated form of this nuclear receptor that does just the opposite. This study showed that shortened RXRα enhances tumor growth by stimulating other proteins that help cancer cells survive. Luckily, the researchers also found that Sulindac can be used to combat this deviant RXRα by switching off its pro-survival function and turning on apoptosis, a process that tells cells to self-destruct.

Sulindac is currently prescribed for the treatment of pain and fever, and to help relieve symptoms of arthritis. The current study demonstrates a new application for Sulindac as a potential anti-cancer treatment that targets truncated RXRα protein in tumors. However, some NSAIDs have gotten a lot of bad press for their potentially dangerous cardiovascular side effects. To overcome this limitation, the researchers tweaked Sulindac, creating a new version of the drug -- now called K-80003 -- that both decreases negative consequences and increases binding to truncated RXRα.

"Depending on the conditions, the same protein, such as RXRα, can either kill cancer cells or promote their growth," Dr. Zhang said. "The addition of K-80003 shifts that balance by blocking survival pathways and sensitizing cancer cells to triggers of apoptosis."

ScienceDaily (June 14, 2010) — Oncogenes are like friends who've gone off the deep end. Normally steady, reliable members of the cellular workforce, these genes become very bad influences when mutated or expressed at high levels -- urging a cell to divide uncontrollably and become cancerous.

Now scientists at the Stanford University School of Medicine and the University of Wuerzburg, Germany, have deciphered a part of the pathway used by a well-known oncogene called Myc to exert its malignant effect. Their findings confirm that at least some cancerous cells have within them the seeds to stop their own growth, if Myc can first be disabled.

They also show for the first time that the cancer cells' dependence on Myc -- a phenomenon called "oncogene addiction" -- is due to a pre-existing, self-regulatory pathway that, in the absence of the oncogene, drives out-of-control cells into a reproductive dead end called cellular senescence. Senescence is a fail-safe mechanism that prevents cells from being able to grow and divide.

"This strongly suggests that cancer cells set up circumstances that allow them to ignore their own internal cues," said Dean Felsher, MD, PhD, associate professor of medicine and of pathology and the leader of the Stanford Molecular Therapeutics Program. "If we can restore that cellular senescence pathway, the tumors stop growing." Felsher is also a member of the Stanford Cancer Center.

The researchers conducted their studies in mice and in cells grown in the laboratory on a specific type of blood-cell cancer called T-cell lymphoma. They found that interfering with an interaction between the Myc protein and another protein called Miz1 significantly limited the ability of the oncogene to cause lymphomas. Shutting off Myc expression restores this cellular senescence pathway and the tumors stop in their tracks. These findings may lead to new ways to fight lymphomas in humans.

The research will be published in the June 15 issue of Genes and Development. In an indication of the collaborative nature of the work, postdoctoral scholar Jan van Riggelen, PhD, from Felsher's lab, shares co-first authorship with graduate student Judith Muller from the University of Wuerzburg and Tobias Otto, PhD, presently at the Dana-Farber Cancer Institute in Boston. Felsher and Martin Eilers, PhD, professor of biochemistry at the University of Wuerzburg, are the senior authors of the study.

The concept of oncogene addiction is not new; in fact, Felsher and his lab members first showed in 2002 and 2004 that turning off Myc expression caused an abrupt and sustained regression in invasive bone and liver cancers in mice. Then, in 2007, they showed that cellular senescence was important to oncogene addiction. But until now no one knew that by shutting off Myc you could make cancer cells actually tell themselves to stop growing.

A clue came during a discussion Felsher had with Eilers, a German colleague and old friend. Members of Eilers' lab at the Theodor Boveri Institute had discovered that lymphoma cells produce and secrete high levels of a self-regulatory molecule called TGF-beta. This was interesting because TGF-beta is known to be an "anti-growth" signal for many types of cells. But it clearly wasn't working in the case of the Myc-expressing lymphoma cells.

"This strongly suggested that the Myc pathway may cause cancer by blocking the ability of TGF-beta to cause cellular senescence," said Felsher. Because a recent study by another lab also implicated TGF-beta in cancer progression, the researchers decided to investigate further to learn how Myc caused cancer and what role TGF-beta might play.

Van Riggelen found that Myc's cancer-causing ability was due to its ability to block the expression of genes that slow or stop a cell's progression through the cell cycle. Without these so-called checkpoint proteins, there's nothing to stop a cell from rushing headlong from one cycle of division to the next.

The researchers also found that Myc relies on Miz1, another protein, to steer it to the appropriate genes; a single mutation in the Myc protein that blocks its ability to bind to Miz1 increases the expression of these checkpoint genes and significantly impedes the protein's ability to cause cancer in laboratory mice. Cells from these lymphomas also displayed more signs of senescence than did cells from tumors with unmutated Myc. But what is it about TGF-beta?

The researchers found that shutting off Myc expression caused the cancer cells to begin to senescence and the tumors to regress -- consistent with the oncogene addiction model (without the Myc oncogene, the cells couldn't maintain their cancerous state). But when the TGF-beta pathway was blocked, the loss of Myc no longer triggered tumor regression.

"We've learned that in order for oncogenes to cause cancer, they have to first interfere with or block the cell's own self-regulatory, or autocrine, pathways," said Felsher. Because these pathways are simply turned off by some oncogenes, he explained, they tend to remain intact even as the cancer progresses. This means that shutting off the right oncogene can flip those pathways back on, or restore the cells' ability to hear their own signals, and may be a key step in fighting many types of cancer.

Felsher and his collaborators are now working with Stanford oncologist and lymphoma expert Ronald Levy, MD, to determine whether the results in mice hold true in human patients. Levy is the Robert K. and Helen K. Summy Professor in the School of Medicine and a member of the Stanford Cancer Center.

Clearly, TGF-beta is critically important in cancer progression. As long as its pathway is active, the cancerous cell remains poised to senesce. But Felsher and others also wonder if there's even more to the story. Might it be possible that the lymphoma cells make, and secrete, so much TGF-beta not to try to put the brakes on their own proliferation, but rather to block the division of other, non-cancerous cells around them? If so, TGF-beta may serve as a way for the cancer cell to clear the stage to allow unimpeded cell division.

"The idea that it's a secreted factor is very exciting," said Felsher. "It could function almost as a way to block other cells that compete with it for space or nutrients. But what it really tells us is that cancer development, and cancer therapies, don't occur in a vacuum. There's a lot of communication among and within cells that we need to understand."

SCIENTISTS have made a discovery about the nature of the proteins involved in cell division which could take them a step closer to cutting deaths from lung cancer.

Researchers at the University of New South Wales and the Pharmacoproteomics Program at the Children's Cancer Institute for Medical Research say the discovery could lead to new ways of approaching treatment of non-small cell lung cancers, which accounts for 80 per cent of all lung cancers.

Scientist say that targeting B3-tubulin, a protein known for maintaining the structural integrity of cells, could be key to increasing drug sensitivity in non-small cell lung cancer.

They found that by suppressing B3-Tubulin it increased the sensitivity of the cancer to standard chemotherapy drugs.

The findings were published in the international journal Cancer Research on Thursday.

The Australian biotech company, Benitec, is currently developing therapeutics focused on specifically blocking B3-tubulin activity.

CHICAGO — The experimental drug PLX4032, which reverses the effects of a mutation found in certain tumors, is considered a prime example of the “targeted” cancer therapies of the future. The drug — the subject of a three-part series in The New York Times in February — produced seemingly miraculous results in some patients with melanoma.

But when the same drug was tried in patients whose colorectal tumors had the same mutation, there was barely any effect, researchers reported here last week at the annual meeting of the American Society of Clinical Oncology.

Same drug, same mutation, different result.

The findings serve as another reminder of how devilishly complex cancer can be and how much more remains to be understood. They provide a sobering check on the enthusiasm that had been building about the targeted therapies, which act to block particular abnormalities that spur tumor growth.

“This is one of the few warning shots over the bow,” said Dr. Scott Kopetz of the M.D. Anderson Cancer Center in Houston, who led the colorectal cancer study.

Indeed, even as researchers at the meeting hailed the latest drug successes, they acknowledged that the path forward was not as easy as once envisioned. Many targeted therapies are failing in clinical trials.

“We’ve gone through a very rapid period of high expectations, maturation and disappointments,” said Dr. J. Leonard Lichtenfeld, the deputy chief medical officer of the American Cancer Society. “I think there was almost a naïveté that if we could find the target, we would have the cure.”

Dr. Kopetz said that after a period of huge gains that culminated with the approval in 2004 of two targeted drugs, Avastin and Erbitux, progress against colon cancer had stalled. “In the past five years I don’t think we’ve made any headway,” he said.

One of the stars of the oncology conference was Pfizer, whose experimental drug crizotinib shrank tumors in nearly all lung cancer patients whose tumors had a particular genetic abnormality. The abnormality was discovered only three years ago, and the drug is moving toward the market.

“It is based on biology and just speaks to the power of understanding the cancer cell,” Dr. Mark G. Kris, a lung cancer specialist at Memorial Sloan-Kettering Cancer Center in New York, said at a news conference.

But Pfizer has had numerous, if less publicized, failures in trials for other targeted therapies. Its kidney cancer drug, Sutent, did not work as a treatment for breast, colon and liver cancers. Another drug that blocks a protein called the insulin-like growth factor receptor — a hot target among drug companies — failed as a lung cancer treatment.

“I was really surprised when the negative results came out,” said Dr. Mace L. Rothenberg, an oncologist who leads Pfizer’s cancer clinical trials.

Conventional chemotherapy typically works by killing rapidly dividing cells. That can mean the tumor but also certain normal cells, causing side effects like hair loss, nausea, diarrhea and anemia.

Targeted therapies, by contrast, aim at proteins that are somehow contributing to tumor growth or survival but, ideally, are not found in healthy cells. That could translate into more effectiveness with fewer side effects.

Numerous targeted drugs are in use and are improving treatment. The paragon is Gleevec, which can keep chronic myeloid leukemia in check for years. Others include Tarceva for lung cancer and Nexavar for kidney and liver cancers.

But the drugs have their own side effects. And in many cases, they work best when used with chemotherapy, so patients cannot escape the side effects of chemo.

Enthusiasts for the targeted drug have been saying for years that tumors will eventually be characterized by their molecular profiles — which mutated genes they have — rather than where in the body they occur. Names like breast cancer and lung cancer will be supplanted by terms like B-RAF-positive or EGFR-positive tumors. And drugs will be chosen based on that profile, the way antibiotics are generally selected based on the pathogen that is causing the infection, not on where in the body the infection occurs.

Massachusetts General Hospital, for instance, is running a clinical trial testing a drug from AstraZeneca on any type of cancer — providing it has a mutation in the gene B-RAF, the same gene that is the target of PLX4032.

But the test of PLX4032 in colon cancer suggests that the location of the tumor still does matter, that it will not be just a case of looking at the target. There are other examples as well. Erbitux and Vectibix do not work in colon cancer patients with a mutation in a gene called K-RAS. But the relationship between the mutation and the effectiveness of Erbitux does not seem to hold in lung cancer.

Experts say that in certain cancers a genetic mutation might be present but is not really driving the cancer, as it might be in other types of cancer.

“You’ve got to target a specific disease, not a biomarker,” said Dr. Mark J. Ratain, an oncologist at the University of Chicago.

Even within the same type of cancer, there can be differences. Researchers reported at the conference that Erbitux, also known as cetuximab, did not prolong survival after surgery for early stage colon cancer, even though the drug works for metastatic colorectal cancer. The failure occurred even though all the patients in the trial were screened to make sure they did not have the mutated K-RAS gene that would have rendered the drug ineffective.

Another study found that in more than 12 percent of cases, tumors that spread to the liver from the breast differed from the original tumor in markers widely used to help determine treatment — estrogen receptor, progesterone receptor or Her2.

The physical characteristics of the drug also matter. Avastin works on the outside of cells to block the action of a protein called VEGF that spurs the formation of blood vessels that nourish tumors. It has prolonged survival in colon cancer and lung cancer.

But so-called small-molecule drugs that try to block the action of VEGF by working on the insides of cells have failed in many trials for lung cancer and colon cancer.

Still, researchers say the setbacks should not be surprising or discouraging but rather part of an effort to learn what makes cancer tick.

“I don’t find it disappointing, said Dr. Robert J. Mayer, a gastrointestinal cancer specialist at the Dana-Farber Cancer Institute in Boston. “I find it intriguing.”

Many researchers say the path forward is to go from merely targeted to truly personalized therapy.

Some leading genetic scientists from Harvard, M.I.T. and the Broad Institute recently helped start a company, Foundation Medicine, that plans to develop a comprehensive test profiling a patient’s tumor, to help doctors personalize therapy.

Some major cancer centers are already doing this on their own, particularly for lung cancer.

At Sloan-Kettering, tumor samples from patients with a certain type of lung cancer are tested for 91 mutations in eight genes. In half the cases, the tests have found a mutation that drives the cancer. In 18 percent of cases, the findings influence the choice of therapy, Dr. Kris said.

The drawback of such a personalized approach is that it will take years to develop drugs for each small subset of patients.

“I think the era of one drug for a whole disease type has passed,” said Dr. Rothenberg, of Pfizer. “We’re going to go where the science leads us. We just have to get smarter about it.”

The phone call that would change Dr. Michael Weitz’s life came from his mother. In June 2009, she tuned in to the evening news and learned about an experimental cancer drug that had made a patient’s lung tumors all but disappear. She phoned her son to say that the drug, a pill called crizotinib, might help him.

Dr. Weitz, an emergency room physician from California who had never smoked cigarettes, needed all the help he could get. Three years earlier, at age 49, the father of three boys had been diagnosed with non-small cell lung cancer (NSCLC), and the disease would eventually invade his bones and his brain. Chemotherapy, surgery, radiation, and erlotinib (Tarceva) had kept him alive, but he never knew when the latest treatment would stop working.

The new drug, however, was a long shot. Fewer than five lung cancers in 100 had the specific genetic change targeted by crizotinib. But because his left lung had been removed, Dr. Weitz had plenty of tumor tissue available for testing. His doctors sent a sample to Massachusetts General Hospital for analysis, and the test came back positive, making him eligible for the treatment.

Dr. Weitz’s tumor cells harbored a fusion of two genes (EML4 and ALK) that appears to drive the disease in some patients. He enrolled in the trial, and 2 months later scans showed a striking reduction in his cancer. By the next round of testing, the tumors had disappeared to the point where doctors described it as “minimal disease.”

“The results were dramatic,” Dr. Weitz said recently. “This was a game-changer.” Compared with his other treatments, he has experienced few, if any, side effects. The beauty of this targeted therapy, he noted, “is that you’re not killing off healthy cells—you’re just going after the bad guys.”

Back to Work

Although he knows the disease could return at any time, Dr. Weitz has returned to work and is once again exercising. He has also joined the scientific advisory board of the Lung Cancer Foundation of America, an organization dedicated to funding research. In part because of this advocacy work, Dr. Weitz traveled to Chicago earlier this month for the annual meeting of the American Society of Clinical Oncology (ASCO).

He was also there to hear a presentation on the crizotinib trial in which he had been participating. The results were featured in the plenary session, which is unusual for small, early-stage trials. But the results were impressive: 87 percent of the 82 patients in the trial responded and many saw their tumors shrink or their disease stabilize after 8 weeks of therapy, the researchers reported.

“This trial confirms what we have known from the very first patient—that this drug is a great option for these patients,” said Dr. Alice Shaw of the Massachusetts General Hospital Cancer Center and an author of the findings. She cautioned, however, that little is known about the natural history of this particular type of lung cancer and additional research is needed.

More than 100 patients have received crizotinib after testing positive for the EML4/ALK fusion gene. Because most patients are still being treated, the trial does not yet have data on survival, noted Dr. Yung-Jue Bang of Seoul National University College of Medicine in Korea, who presented the findings.

In a discussion of the results at the plenary session, Dr. Martin Edelman of the University of Maryland Greenebaum Cancer Center noted the drug’s “striking activity” and the “durable” responses in patients who had already received multiple therapies. “It’s hard to imagine that these early results will change over time,” he said.

Biological Markers

Dr. Edelman also provided some historical context. Six years ago, when doctors first observed dramatic responses to gefitinib (Iressa) in patients with lung cancer, there were no molecular markers for identifying likely responders. It was only by analyzing patient samples retrospectively that researchers discovered biomarkers of response (mutations in the EGFR gene).

Crizotinib has followed a different path. The EML4/ALK fusion gene, which produces an aberrantly activated ALK protein, is used as a marker to select patients. The drug was initially developed to inhibit a signaling protein called c-Met, but it also proved to be active against the ALK protein, another signaling protein and, like c-Met, a tyrosine kinase.

When Japanese researchers reported the presence of the fusion gene in lung tumors in August 2007, the drug was already being evaluated in other cancers. Researchers at Massachusetts General Hospital quickly developed a test for the fusion gene. Within months, they had enrolled a patient with lung cancer into the trial, and in less than 3 years, preliminary results from the trial were making news.

“This study demonstrates the power of understanding the biology of cancer,” said Dr. Mark Kris, chief of the Thoracic Oncology Service at Memorial Sloan-Kettering Cancer Center, who was not involved in the study. Crizotinib, he continued, is an example of what doctors have always wanted to give their patients—a drug that is tailored to the specific features of a given patient’s disease.

At the ASCO meeting, some lung cancer experts were discussing crizotinib as a model for moving forward in this deadly disease. By discovering genetic alterations underlying subtypes of lung cancer and developing therapies against these changes, the researchers hoped to make progress against this leading cause of cancer death worldwide.

In the case of crizotinib, testing patient tumors was critical for uncovering the drug’s dramatic effects in selected patients. Had the drug been tested in 100 unselected patients with lung cancer, researchers might have concluded that the drug had little or no activity in the disease.

Dr. Edelman stressed the importance of selecting patients in trials of targeted drugs by showing a slide with a long list of disappointing lung cancer trials. “If targeted drugs had been employed in targeted populations, how many of these trials would have been positive?” he asked.

Larger crizotinib trials are planned or underway, including a phase III study called PROFILE 1007. This will compare crizotinib with standard second-line chemotherapy for patients with ALK fusion gene-positive recurrent NSCLC.

A Unique Disease

Last year, Dr. Shaw and her colleagues reported that patients with the EML4/ALK fusion gene had a distinct subtype of NSCLC with identifiable clinical characteristics. These patients, like Dr. Weitz, tend to be much younger than other patients with lung cancer, to be nonsmokers, and to have the adenocarcinoma form of the disease.

The patients also have a high likelihood of responding to ALK-targeted agents, although not all patients with the fusion gene respond to crizotinib. In addition, some patients with the gene fusion have developed resistance to the drug, the researchers said.

Still, many patients are doing well (at least one patient has been on the drug for 20 months). With more than 200,000 new lung cancers diagnosed in the United States each year, an estimated 10,000 patients could be eligible for these agents. “It’s our job as oncologists to find these patients,” said Dr. Kris.

A project launched last fall called the Lung Cancer Mutation Consortium could play a role. Fourteen sites around the country will test patients free of charge for a panel of 10 genetic changes for which there are drugs available, including the EML4/ALK fusion gene. Patients will be referred to the appropriate clinical trials based on their particular tumor types.

The 2-year consortium project, funded with a $5.2 million grant from the American Recovery and Reinvestment Act, aims to determine the frequencies of certain mutations in 1,000 patients with advanced lung adenocarcinomas. Investigators will also collect clinical information to uncover links between specific mutations and clinical features and outcomes.

“The consortium is how we will translate findings from our research on the human genome into medicines for patients,” said Dr. Paul Bunn, former director of the University of Colorado Cancer Center and a project leader. He noted that The Cancer Genome Atlas project, for instance, is characterizing genomic changes in two types of lung cancer and that these results will be used to develop biomarker-driven therapies.

“A Future Again”

In his work advocating for lung cancer research, Dr. Weitz urges patients to have their tumors tested, saying that this can help them develop a strategy for trying to manage the disease in a way that other chronic diseases are managed.

He compares being a patient to playing chess. “You have to think several steps ahead,” he explained. “And you always need several therapies in your back pocket in case the current one doesn’t work out.”

These days, though, he has more than just cancer on his mind. “My friends and family have been so supportive,” he said. “For more than 3 years, there’s been an outpouring of love and affection. I now have energy and can think about planning trips. I have a future again.”

LONDON: Ten years after Tony Blair and Bill Clinton announced that scientists had deciphered the book of life, many of the predicted benefits of unravelling the human genome are still to be realised.

Yet as researchers prepare to mark the 10th anniversary of the completion of the first draft of the human genome, they claim to be poised on the edge of a development that will bring benefits of the $3.4 billion project to everyone.

Hidden within our DNA, they say, are the secrets that will teach us how to live a healthy life. Geneticists have discovered that the malfunctioning genes that cause major diseases, including cancer, heart disease and diabetes, also carry distinctive signatures that can reveal what caused the malfunctions in the first place.

''We can look at the genome of a cancer cell and we can see writ, as a kind of archaeological record, what caused those mutations maybe 20 or 30 years ago,'' said Mike Stratton, the director of the Wellcome Trust Sanger Institute, the British arm of the efforts to sequence the genome.

The Sanger Institute is leading efforts to sequence the genomes of cancer cells taken from 25,000 patients in an attempt to unravel the full repertoire of genetic differences that make cancerous tissue different from healthy tissue.

Researchers have been able to compare the DNA taken from a lung cancer cell with that of a healthy cell and prove it carries a set of differences that reveal the cancer was caused by smoking.

As they peer deeper into the genome for more of these telltale signatures, they hope they will be able to provide some definitive answers about the things that are good and bad for our health.

They may even be able to answer debates about whether chocolate, coffee and red wine are harmful or beneficial. Scientific studies have produced conflicting results.

Professor Stratton said: '' This is going to be transforming.''

The completion of the first draft of the full sequence of the human genome on June 26, 2000, was the culmination of 10 years of work and the contribution of hundreds of scientists. This week the Science Museum in London will open an exhibition detailing some of the achievements since that date. Before the publication of the genome, biologists believed our DNA would contain hundreds of thousands of genes needed to provide all the building blocks that make up the human body.

But the human genome project discovered there were just 22,000 genes. It did not seem enough to explain our complex nature. A parasite made up of a single cell, called a trichomoniasis, has been found to have three times as many genes in its genome.

June 21, 2010 (Barcelona, Spain) — Epigenetic abnormalities appear to be a new therapeutic target for a range of cancers. Low doses of demethylating agents used in combination appear to induce lung cancer cells to become less malignant, according to data from trials of advanced lung cancer patients.

Presenting his preliminary results here at the 15th Congress of the European Hematology Association (EHA), Stephen Baylin, MD, deputy director of the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University in Baltimore, Maryland, explained evidence suggesting that, in preclinical studies, low, less toxic doses of 5-azacytidine (Vidaza, Celgene) and 5-aza-2'-deoxycytidine (Dacogen, Eisai), work by reprogramming tumor cells to revert to a less tumorigenic state. Full results have been submitted to a medical journal.

These drugs, used at much lower doses than when they were originally introduced, have been used in the preleukemic disease myelodysplasia since the 1990s, and are now approved by the US Food and Drug Administration (FDA) for this purpose. Now, low doses of these drugs are being combined with histone deacetylase inhibitors (HDACIs) in trials for myelodysplasia, acute myelogenous leukemia, and — very recently — for nonsmall-cell lung carcinoma, a solid tumor.

"In our lab, we have found that you can use low doses of the 2 demethylating drugs together to boost gene function when followed by HDACIs; these combinations are in clinical trials," Dr. Baylin told Medscape Hematology.

He explained that by using low doses of drugs like 5-azacytidine and 5-aza-2'-deoxycytidine, it is possible to separate the killing effects of these drugs from the reprogramming effect, in which cancer cells are given a new "memory" to convert them to a less tumorigenic state.

"We will have a very exciting time over the next 3 years. We're learning to improve therapy for leukemia with these drugs by [changing] how we give them in terms of dose and timing; in addition, we are now gaining traction in solid tumors. There's a lot of excitement in patients with advanced lung cancer who have failed previous chemotherapy," he noted.

Dr. Baylin added that a subset of these patients — in early results from a trial being conducted by his colleagues at Johns Hopkins University, Charles Rudin, MD, and Ros Juergens, MD — are showing robust responses with stable or remission rates totaling up to 30%. "Some responses are lasting up to a year or more in a setting where one would usually only expect about 4 months after failing chemotherapy," Dr. Baylin announced.

These findings have led to the planning of intensive trials, under the aegis of the Stand Up to Cancer program, in a joint venture with the American Association for Cancer Research, which are scheduled to begin over the next 3 years in lung, colon, and breast cancer.

Robin Foa, MD, president of EHA and head of the Division of Hematology at Sapienza University in Rome, Italy, said that hematology is often a front-runner in innovative forms of management from diagnosis to prognosis and treatment.

"This research is a further step forward in the treatment of hematological malignancies. As hematologists, we are often a step ahead, and we've known this for many years. For example, in Philadelphia-positive acute lymphoblastic leukemia, the worst disease in hematology, if not in medicine, we can now put patients into remission even at 80 to 90 years of age without chemotherapy, just with a tyrosine kinase inhibitor."

Commenting on Dr. Baylin's work, Dr. Foa said: "What we have just heard is a further development that has stemmed from knowledge in the field of epigenetics, and it is likely that in the near future, whole genome sequencing will further change the management of patients with hematological malignancies."

NEW YORK (CBS) Can certain painkillers cause cancer cells to commit suicide?

That's the suggestion of a new study of a popular anti-inflammatory drug known as sulindac, published June 15 in the journal Cancer Cell. The drug is marketing as Clinoril.

Scientists have long known that cancer is less common in people who take aspirin and other nonsteriodal anti-inflammatory drugs (NSAID), according to a statement issued by Sanford-Burnham Medical Research Institute in La Jolla, Calif., where the study was conducted.

The study offers an explanation of why this happens.

It showed that sulindac - which is commonly prescribed to treat pain and fever and to ease arthritis symptoms - triggers cell death by binding to a protein called RXR-alpha that travels into the nucleus and signals genes to turn on or off.

In essence, the cells kill themselves, according to the report.

"Sulindac has a very strong impact on cancer activity," said Xiao-kun Zhang, Ph.D., a professor at Sanford-Burnham and senior author of the study. He said NSAIDs have shown to inhibit the growth of many kinds of cancer, including colon, breast, prostate, and lung. "Our study might help drug makers develop new drugs with anticancer activity."

NSAIDs have gotten a lot of bad press for causing potentially dangerous cardiovascular side effects. To overcome this limitation, the researchers created a new version of sulindac - called K-80003 - that helps diminish side effects, according to the statement.

ELEANOR HALL: The latest scorecard on Australia's health is in, and it contains some mixed and somewhat mysterious results.

We're living longer and the number of deaths from cardiovascular disease is down. But, despite a drop in the smoking rate, more Australians are getting cancer.

And the mental health of young people continues to cause concern, as Ashley Hall reports from Canberra.

ASHLEY HALL: Healthcare in Australia is a $100 billion a year industry.

PENNY ALBON: Seventy per cent of that comes from your taxes and another 30 per cent you pay from your back pocket.

ASHLEY HALL: Doctor Penny Albon is the director of the Australian Institute of Health and Welfare, which produced the latest national report card on Australia's health. And she says health costs are growing.

PENNY ALBON: The Medicare data shows that benefits for people going to GPs increased in 2008/9 well above the population increase, almost a 6 per cent increase. Hospital admissions rose by 37 per cent in the decade to 2007/8 and they’re still increasing.

ASHLEY HALL: Is it clear what's driving that?

PENNY ALBON: I think as our health improves our expectations of the system increase. And as medical technology comes up with new and better ways to treat people and as outcomes from treatment improve that supply really does drive a demand in the population.

ASHLEY HALL: The report shows that all that money is providing some better outcomes. The life expectancy of Australians at birth is among the highest in the world - almost 84 years for women and 79 years for men.

And the survival rate for Australia's biggest killer, cardiovascular disease is improving.

PENNY ALBON: The death rate has dropped by 76 per cent since it peaked in the late 1960s and interestingly less than a quarter of the deaths are among people aged under 75 years. So that means it's gradually becoming an older person's disease.

ASHLEY HALL: The death rate attributed to cancer is also on the improve; although the report forecasts a rise in new diagnoses this year. It's an element of the report that's caught the eye of the Health Minister Nicola Roxon.

NICOLA ROXON: There is a worrying trend that is in this report, which shows that this year we can expect 115,000 Australians to be diagnosed with cancer and that is a 10 per cent increase from 2006 - a very big jump. So cancer is an area where we have to continue the fight.

ASHLEY HALL: Nicola Roxon says the Government's $650 million investment in regional cancer centres this year should help address the problem, although the Cancer Council says even more needs to be done.

The Health Minister says more is being done in the area of youth mental health.

NICOLA ROXON: Among young people we still have the very worrying trends that we are not treating a large number of people who have their first mental health instance, particularly in their adolescence. That's why as part of our health reform package we are actually focusing on youth mental health services.

Expanding the number of headspace services for example across the country so that 20,000 more young people can get support. There is always going to be a lot more for us to do and the report released today actually provides us with a lot of information to be able to map out those future decisions.

ASHLEY HALL: But the Federal Government's most senior independent mental health adviser, John Mendoza, has quit his post, citing frustration over what he says is the Government's lack of vision and commitment to the mentally ill.

And the Australian of the Year and Professor of youth mental health at the University of Melbourne, Patrick McGorry says the expansion of services the Minister points to is only about a tenth of what's required.

PATRICK MCGORRY: If the investment were of the order of 100 million for headspace per annum and 100 million to begin to assemble a backup system, the early psychosis backup system for headspace, so that's a total of about 200 to 250 million recurrent, a year we think of all up.

Now that's not a huge amount of money, but it does contrast with the roughly about 26 million per year that is currently being allocated in the last budget. So they're off the page by a factor of ten really.

ASHLEY HALL: The report finds Australia's level smoking continues to fall, it's among the lowest in the OECD, with only one in six adults smoking daily. And that's produced a commensurate drop in diseases associated with the habit.

[comment - there is no mystery regarding increased rates of cancer or any other chronic disease. Despite our good health report this masks that all the major risk factors for chronic disease are increasing. We are living longer, but are we healthy? Note the rise in hospital admissions]

ScienceDaily (June 22, 2010) — Showing movies in 3-D has produced a box-office bonanza in recent months. Could viewing cell behavior in three dimensions lead to important advances in cancer research? A new study led by Johns Hopkins University engineers indicates it may happen. Looking at cells in 3-D, the team members concluded, yields more accurate information that could help develop drugs to prevent cancer's spread.

The study, a collaboration with researchers at Washington University in St. Louis, appears in the June issue of Nature Cell Biology.

"Finding out how cells move and stick to surfaces is critical to our understanding of cancer and other diseases. But most of what we know about these behaviors has been learned in the 2-D environment of Petri dishes," said Denis Wirtz, director of the Johns Hopkins Engineering in Oncology Center and principal investigator of the study. "Our study demonstrates for the first time that the way cells move inside a three-dimensional environment, such as the human body, is fundamentally different from the behavior we've seen in conventional flat lab dishes. It's both qualitatively and quantitatively different."

One implication of this discovery is that the results produced by a common high-speed method of screening drugs to prevent cell migration on flat substrates are, at best, misleading, said Wirtz, who also is the Theophilus H. Smoot Professor of Chemical and Biomolecular Engineering at Johns Hopkins. This is important because cell movement is related to the spread of cancer, Wirtz said. "Our study identified possible targets to dramatically slow down cell invasion in a three-dimensional matrix."

When cells are grown in two dimensions, Wirtz said, certain proteins help to form long-lived attachments called focal adhesions on surfaces. Under these 2-D conditions, these adhesions can last several seconds to several minutes. The cell also develops a broad, fan-shaped protrusion called a lamella along its leading edges, which helps move it forward. "In 3-D, the shape is completely different," Wirtz said. "It is more spindlelike with two pointed protrusions at opposite ends. Focal adhesions, if they exist at all, are so tiny and so short-lived they cannot be resolved with microscopy."

The study's lead author, Stephanie Fraley, a Johns Hopkins doctoral student in Chemical and Biomolecular Engineering, said that the shape and mode of movement for cells in 2-D are merely an "artifact of their environment," which could produce misleading results when testing the effect of different drugs. "It is much more difficult to do 3-D cell culture than it is to do 2-D cell culture," Fraley said. "Typically, any kind of drug study that you do is conducted in 2D cell cultures before it is carried over into animal models. Sometimes, drug study results don't resemble the outcomes of clinical studies. This may be one of the keys to understanding why things don't always match up."

Fraley's faculty supervisor, Wirtz, suggested that part of the reason for the disconnect could be that even in studies that are called 3-D, the top of the cells are still located above the matrix. "Most of the work has been for cells only partially embedded in a matrix, which we call 2.5-D," he said. "Our paper shows the fundamental difference between 3-D and 2.5-D: Focal adhesions disappear, and the role of focal adhesion proteins in regulating cell motility becomes different."

Wirtz added that "because loss of adhesion and enhanced cell movement are hallmarks of cancer," his team's findings should radically alter the way cells are cultured for drug studies. For example, the team found that in a 3-D environment, cells possessing the protein zyxin would move in a random way, exploring their local environment. But when the gene for zyxin was disabled, the cells traveled in a rapid and persistent, almost one-dimensional pathway far from their place of origin.

Fraley said such cells might even travel back down the same pathways they had already explored. "It turns out that zyxin is misregulated in many cancers," Fraley said. Therefore, she added, an understanding of the function of proteins like zyxin in a 3-D cell culture is critical to understanding how cancer spreads, or metastasizes. "Of course tumor growth is important, but what kills most cancer patients is metastasis," she said.

To study cells in 3-D, the team coated a glass slide with layers of collagen-enriched gel several millimeters thick. Collagen, the most abundant protein in the body, forms a network in the gel of cross-linked fibers similar to the natural extracellular matrix scaffold upon which cells grow in the body. The researchers then mixed cells into the gel before it set. Next, they used an inverted confocal microscope to view from below the cells traveling within the gel matrix. The displacement of tiny beads embedded in the gel was used to show movement of the collagen fibers as the cells extended protrusions in both directions and then pulled inward before releasing one fiber and propelling themselves forward.

Fraley compared the movement of the cells to a person trying to maneuver through an obstacle course crisscrossed with bungee cords. "Cells move by extending one protrusion forward and another backward, contracting inward, and then releasing one of the contacts before releasing the other," she said. Ultimately, the cell moves in the direction of the contact released last.

When a cell moves along on a 2-D surface, the underside of the cell is in constant contact with a surface, where it can form many large and long-lasting focal adhesions. Cells moving in 3-D environments, however, only make brief contacts with the network of collagen fibers surrounding them-contacts too small to see and too short-lived to even measure, the researchers observed.

"We think the same focal adhesion proteins identified in 2-D situations play a role in 3-D motility, but their role in 3-D is completely different and unknown," Wirtz said. "There is more we need to discover."

Fraley said her future research will be focused specifically on the role of mechanosensory proteins like zyxin on motility, as well as how factors such as gel matrix pore size and stiffness affect cell migration in 3-D.

A targeted therapy that has generated excitement for its early success in breast cancer is now being tested on other cancers, including often-deadly ovarian tumors.

Doctors and patients have eagerly anticipated the drugs, which provide an entirely new route to killing tumors that is less toxic than traditional chemotherapies.

Called PARP inhibitors, after the enzyme they target, the drugs disable a key mechanism that cancer cells employ to repair themselves. Used in combination with current drugs against breast cancer, PARP inhibitors were shown to add cancer-free months to patients' lives while causing few serious side effects.

Although many cancer treatments have shown early promise only to fade under wider scrutiny, the prospect of a whole new approach has generated buzz even in staid journals such as The New England Journal of Medicine. Last year, the journal editorialized on the strength of the small breast-cancer trial.

Since then, enthusiasm has only grown, with patients eagerly volunteering for limited spots in clinical trials to gain access to the treatment.

"There are a lot of patients very interested in this," said Dr. Linda Van Le, an oncologist at the University of North Carolina-Chapel Hill who is helping enroll patients in a clinical trial of a PARP drug for ovarian cancer.

At least nine PARP inhibitor drugs are in different phases of the U.S. Food and Drug Administration approval process, but none is yet on the market.

As a result, patients can get the drugs only through clinical trials. In addition to the ovarian-cancer study at UNC-Chapel Hill, trials are on tap there for lung, breast and colorectal cancers. Doctors at Duke University will soon participate in a PARP inhibitor trial aimed at colon cancer.

Lynn Burrell, 44, of Clayton, N.C., was the first to enroll in the ovarian-cancer study at N.C. Cancer Hospital in Chapel Hill, which was initially approved to enroll three patients. Van Le said her group quickly filled its quota and was allowed to enlist seven more patients. The trial is led by the drug's manufacturer, Abbott Laboratories.

After being diagnosed with ovarian cancer last year, Burrell had a hysterectomy and chemotherapy. When tumors recently returned in nearby tissue, she seized the chance to try the experimental treatment.

"I was excited about it," Burrell said. "Knowing there are limited chemotherapies for ovarian cancer, this was a great opportunity."

PARP inhibitors work in a way far different from traditional chemotherapies, which wipe out cancer cells but also kill or damage healthy cells. That residual damage is what causes many of chemo's dreaded side effects - hair loss, nausea, muscle weakness and fatigue.

The new approach, which stems from discoveries about the genetic source of tumors, is much more focused.

It was initially developed to capitalize on a gene mutation evident in some inherited cancers, notably breast cancers associated with the BRCA1 and BRCA2 genes. Women who inherit these damaged genes are five times as likely to develop breast cancer and at least 11 times as likely to have ovarian cancer. Men who inherit the mutations are at increased risk for breast, pancreatic and prostate cancers.

Both BRCA1 and BRCA2 are normally helpful genes involved in repairing damaged cells. With the harmful mutation, however, they don't function, so damaged cells grow out of control, building tumors.

Teams from Duke University Medical Centre in Durham, North Carolina, and the University of Toronto studied 1,319 men who had surgery.
Of these, 236 – around a fifth - were taking statins at the time they had their prostate gland removed.

For men taking a dose equivalent to 20 milligrams of simvastatin a day, recurrence risk was reduced by 43 per cent. Simvastatin is one of the most widely used statin drugs.

Men taking doses higher than 20 milligrams reduced their risk by half, while those taking less than 20 milligrams saw no benefit.

Dr Stephen Freedland, of Duke University, said: ‘The findings add another layer of evidence suggesting that statins may have an important role in slowing the growth and progression of prostate cancer.

‘Previous studies have shown that statins have anti-cancer properties, but it's not entirely clear when it's best to use them - or even how they work.’
There were differences between men who took the drugs and those who did not, the researchers pointed out.

Statin users tended to be white, older and heavier than non-users. They also had lower clinical stages at diagnosis, but higher scores of cancer aggressiveness.

Dr Robert Hamilton, from the University of Toronto in Canada, said: ‘These findings are intriguing, but we do need to approach them with some caution.

‘For example, we don't know the diet, exercise or smoking habits of these men. So it's not entirely clear if the lower risk we detected is related to the statins alone - it could be due to other factors we were not able to measure.
‘We do feel, however, that based on these findings and those from other studies, the time is ripe to perform a well-controlled randomised trial to test whether statins do indeed slow prostate cancer progression.’
Each year around 35,000 men are diagnosed with prostate cancer in the UK, and 10,000 die from the disease.

Dr Kate Holmes, research manager at The Prostate Cancer Charity, said: ‘This study looks at how levels of the protein PSA in the blood, an indicator of whether prostate cancer has returned in men who have undergone treatment for the disease, are affected by the use of statins. The results show that those men who were taking statins had a 30 per cent lower risk of their cancer recurring. The researchers also discovered that men using statins who did not have the disease also experienced a small decline in their PSA.

‘However, there are still many unanswered questions about the use of statins and researchers and doctors must be cautious in linking low levels of PSA in men taking statins with the belief that cancer has not returned. It could be that whilst statins are effective in reducing PSA levels, they may have little effect on whether prostate cancer is likely to return.

‘It is too soon to say whether the results of this study could lead to a potential breakthrough in the use of statins to manage or reduce the risk of prostate cancer. However, the results of the research do beg the need for further studies to determine whether the use of statins can indeed reduce the chances of prostate cancer returning, rather than purely suppressing PSA levels.

‘Although the use of statins, a common treatment to lower cholesterol, has a variety of health effects, there has been much debate surrounding the effects of statins on men with prostate cancer. This new research is an interesting step forward in helping us to understand the role that statins could play in reducing the risk of prostate cancer.
‘Any man who does have concerns about taking statins should discuss it further with their GP.’

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